Yuncai Chen

TL;DR: It is demonstrated that a period of early-life “psychological” stress causes late-onset, selective deterioration of both complex behavior and synaptic plasticity in middle-aged, but not young adult, rats exposed to fragmented maternal care during the early postnatal period.

TL;DR: It is found that CRH expression is augmented in hippocampus of middle-aged CES rats, and whether the morphological defects and poor memory performance in these animals involve excessive activation of CRF1 receptors is tested, suggesting that persistently elevated hippocampal CRH–CRF1 interaction contributes importantly to the structural and cognitive impairments associated with early-life stress.

TL;DR: This paper showed that a short period of stress early in life can lead to delayed, progressive impairments of synaptic and behavioral measures of hippocampal function, with potential implications to the basis of age-related cognitive disorders in humans.

TL;DR: A novel concept regarding the origin of toxic early-life stress is introduced, stating that it may derive from specific patterns of environmental signals, especially those derived from the mother or caretaker.

TL;DR: A novel, activity-dependent transcriptional regulation of HCN molecules by developmental seizures is demonstrated, which result in long-lasting alteration of the HCN phenotype of specific hippocampal neuronal populations, with profound consequences on the excitability of the hippocampal network.